- Email: [email protected]
Residual heterozygosity in inbred mouse strains
6
References 1 Crewther, P. and Warner, N. L. (1972) Aust. J. Exp, Biol. Med. Sd. 50, 625-635 2 Ebersole,J. L., Tanbman, M. A. and Smith, D.J. (1979) Immunology 36, 649-657 3 Clough, J. D., Minas, L. H. and Strober, W. (1971)J. Immunol. 106, 1624-1629 4 Ebersole, J. L., Tanbman, M. A. and Smith, D.J. (1979)J. Immunol. 123, 19-24
Residual heterozygosity in inbred mouse strains SIR,
Donald W. Bailey (Immunol. Today, 1982, Vol. 3, pp. 210-214) drew attention to the problem of the purity of inbred strains of mice. Twenty-five years ago there was much debate as to whether the immunogenicity of transplanted tumours might be due to impurity in the inbred animals then available. After the demonstration of Klein et aL 1 that immunity to a chemically induced tumour could be detected in the original host, thus eliminating the possibility of transplantation artefacts, imperfections in inbreeding were no longer considered to be of importance. However, there is reason to suspect that the weak immunogenicity of
Immunology Today, vol. 5, No. 1, 1984 5 Elson, C. O., Yarehoan, R., Gracff, A. and Strober, W. (1980) Fed. Proc Fed. Am. Soc. Exp. Biol. 39, 916 6 Trefts, P. E., Riviers, D. A. and Kagnoff, M. E. (1981) Nature(London) 292 7 Mond, J. J., Farrar, J., Paul, W. E. a a/. (1983)J. Immunol. 131,633-637 8 Mond, J. J., Mongini, P. K. A., Sieckmann, D. and Paul, W. E. (1980)J. Immunol. 125,
1066-1070 9 Kung, J. T. and Panl, W. E. (1983) Immunol. Today 4, 37-41 10 Ginis, S., Baker, P. E., Union, N. A. and Smith, K. A. (1979)J. Exp. Med. 149, 1460-1470 11 Eldridge, J. H., Kiyonu, H., Michalek, S. M. and McGhee, J. R. (1983)J. Exp. Med, 157, 789-794
cellophane-ftim-induced tumours and some spontaneous tumours might be due to residual heterozygosity 2. If this hypothesis is correct we might expect to find cases where spontaneous tumours tested early in the history of an inbred strain before inbreeding was complete were immunogenic, but where tumours tested later were not. A beautiful example vindicating this prediction is to be found in the work of Middle and Embleton 3 who found that 28 spontaneous tumours which arose in inbred rats after 1976 were non-immunogenic, whereas previously about a third of tested tumours had displayed immunogenicity. The definition of 'early in the history of the strain' must be modified in view of Bailey's clear demonstration that a minimum of 40 generations of inbreeding are necessary
to reach the point where inbreeding balances mutation, not 20 as is widely believed. Perhaps all claims that spontaneous tumours are immunogenic in the strain of origin should be re-examined in the light of these considerations. O. C. A. SCOTT
Richard lh'mbleby Department of CancerResearctg St Thomas 's Hospital Medical School, London SE1 7EH, UK.
References 1 Klein, G., SjSrgren, H. O. Klein, E. and Hellstr6m, K. E. (1960) Carver Res. 20, 1561-1572 2 Scott, O. C. A. (1980) Br.J. Cancer41, Suppl. IV, 112-117 3 Middle, J. G. and Embleton, M. J. (1981)J. Natl CancerInst. 67, 637-643
References 1 Crewther, P. and Warner, N. L. (1972) Aust. J. Exp, Biol. Med. Sd. 50, 625-635 2 Ebersole,J. L., Tanbman, M. A. and Smith, D.J. (1979) Immunology 36, 649-657 3 Clough, J. D., Minas, L. H. and Strober, W. (1971)J. Immunol. 106, 1624-1629 4 Ebersole, J. L., Tanbman, M. A. and Smith, D.J. (1979)J. Immunol. 123, 19-24
Residual heterozygosity in inbred mouse strains SIR,
Donald W. Bailey (Immunol. Today, 1982, Vol. 3, pp. 210-214) drew attention to the problem of the purity of inbred strains of mice. Twenty-five years ago there was much debate as to whether the immunogenicity of transplanted tumours might be due to impurity in the inbred animals then available. After the demonstration of Klein et aL 1 that immunity to a chemically induced tumour could be detected in the original host, thus eliminating the possibility of transplantation artefacts, imperfections in inbreeding were no longer considered to be of importance. However, there is reason to suspect that the weak immunogenicity of
Immunology Today, vol. 5, No. 1, 1984 5 Elson, C. O., Yarehoan, R., Gracff, A. and Strober, W. (1980) Fed. Proc Fed. Am. Soc. Exp. Biol. 39, 916 6 Trefts, P. E., Riviers, D. A. and Kagnoff, M. E. (1981) Nature(London) 292 7 Mond, J. J., Farrar, J., Paul, W. E. a a/. (1983)J. Immunol. 131,633-637 8 Mond, J. J., Mongini, P. K. A., Sieckmann, D. and Paul, W. E. (1980)J. Immunol. 125,
1066-1070 9 Kung, J. T. and Panl, W. E. (1983) Immunol. Today 4, 37-41 10 Ginis, S., Baker, P. E., Union, N. A. and Smith, K. A. (1979)J. Exp. Med. 149, 1460-1470 11 Eldridge, J. H., Kiyonu, H., Michalek, S. M. and McGhee, J. R. (1983)J. Exp. Med, 157, 789-794
cellophane-ftim-induced tumours and some spontaneous tumours might be due to residual heterozygosity 2. If this hypothesis is correct we might expect to find cases where spontaneous tumours tested early in the history of an inbred strain before inbreeding was complete were immunogenic, but where tumours tested later were not. A beautiful example vindicating this prediction is to be found in the work of Middle and Embleton 3 who found that 28 spontaneous tumours which arose in inbred rats after 1976 were non-immunogenic, whereas previously about a third of tested tumours had displayed immunogenicity. The definition of 'early in the history of the strain' must be modified in view of Bailey's clear demonstration that a minimum of 40 generations of inbreeding are necessary
to reach the point where inbreeding balances mutation, not 20 as is widely believed. Perhaps all claims that spontaneous tumours are immunogenic in the strain of origin should be re-examined in the light of these considerations. O. C. A. SCOTT
Richard lh'mbleby Department of CancerResearctg St Thomas 's Hospital Medical School, London SE1 7EH, UK.
References 1 Klein, G., SjSrgren, H. O. Klein, E. and Hellstr6m, K. E. (1960) Carver Res. 20, 1561-1572 2 Scott, O. C. A. (1980) Br.J. Cancer41, Suppl. IV, 112-117 3 Middle, J. G. and Embleton, M. J. (1981)J. Natl CancerInst. 67, 637-643